Clarification of the molecular mechanism and development of novel nutritional therapy of reticular dysgenesis as mitochondrial disease

2015 Fiscal Year Final Research Report

• Project/Area Number: 25750042
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Eating habits
• Research Institution: The University of Tokushima
• Principal Investigator: TANIMURA Ayako 徳島大学, 大学院医歯薬学研究部, 助教 (10610199)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: AK2 / ATP / ROS / UPR / 好中球 / 細胞分化 / 細網異形成症 / ミトコンドリア

Outline of Final Research Achievements

Adenylate kinase 2 (AK2) is an energy-metabolic enzyme in mitochondrial intermembrane space. We studied about the mechanism of neutrophil differentiation arrest by AK2 deficiency in reticular dysgenesis. By analyzing macrophage and neutrophil differentiation using HL-60 cell line, we found that AK2 is essential for neutrophil differentiation and AK2 knockdown caused increased ROS production. Additionally, differentiation- and stage-specific activation of unfolded protein response (UPR) was observed during macrophage and neutrophil differentiation. We found that differentiation-specific UPR may be required for each differentiation. These results provided important hints to develop a new therapy for reticular dysgenesis.

Free Research Field

栄養学、生化学、細胞生物学